In experiments performed thus far utilizing stumptail macaques (Macaca arctoides), a non-human primate, we have demonstrated that experimentally induced hypertension superimposed on atherogenic diet significantly increases the atherogenic effect of the diet. Recent experiments have shown that when renal hypertension and an atherogenic diet were maintained for six months and the monkeys were then assigned to several therapeutic groups, favorable results on the regression of lesions were obtained by deleting the atherogenic diet, whereas the effect of drug treatment of hypertension alone was questionable. Indeed, continuation of the atherogenic diet combined with an hypertensive drugs, yielded the least favorable results on aortic and coronary atherogenesis. The objectives of the proposed studies are to produce persistent hypertension by a modified unilateral Goldblatt procedure. After the induction phase of combined hypertension and diet-induced atherosclerosis, therapy is to be compared between a) nephrectomy of the ischemic kidney to relieve hypertension, and b) antihypertensive drug treatment without nephrectomy, both with and without continuation of the atherogenic diet. The anti-hypertensive drugs used will be screened in separate experiments on normotensive monkeys given the identical atherogenic diet to determine their intrinsic pharmacologic effects on aortic and coronary atherosclerosis, independent of their blood pressure lowering effects. It is hoped that these experiments will help to explain how and why hypertension accelerates atherogenesis and whether treatment of elevated @rterial pressure without regard to pathogenesis will prevent progression of coronary disease. In separate studies we intend to study the effects of renal hypertension per se on the morphology of blood vessels, without the influence of an atherogenic diet. In addition, later we plan to study the effects of an atherogenic diet on monkeys after successful treatment of long term hypertension to determine whether pre-existing hypertension predisposes the vascular wall to lipid deposition and the development of atherosclerosis.